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Hydrogen Sulfide, Nitric Oxide, and Neurodegenerative Disorders Sandesh Panthi1*, Sumeet Manandhar2 and Kripa Gautam3

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Hydrogen Sulfide, Nitric Oxide, and Neurodegenerative Disorders Sandesh Panthi1*, Sumeet Manandhar2 and Kripa Gautam3 Panthi et al. Translational Neurodegeneration (2018) 7:3 https://doi.org/10.1186/s40035-018-0108-x REVIEW Open Access Hydrogen sulfide, nitric oxide, and neurodegenerative disorders Sandesh Panthi1*, Sumeet Manandhar2 and Kripa Gautam3 Abstract Hydrogen Sulfide (H2S) and Nitric Oxide (NO) have become recognized as important gaseous signaling molecules with enormous pharmacological effects, therapeutic value, and central physiological roles. NO is one of the most important regulators of the pathophysiological condition in central nervous system (CNS). It is critical in the various functioning of the brain; however, beyond certain concentration/level, it is toxic. H2S was regarded as toxic gas with the smell like rotten egg. But, it is now regarded as emerging neuroprotectant and neuromodulator. Recently, the use of donors and inhibitors of these signaling molecules have helped us to identify their accurate and precise biological effects. The most abundant neurotransmitter of CNS (glutamate) is the initiator of the reaction that forms NO, and H2Sishighly expressed in brain. These molecules are shedding light on the pathogenesis of various neurological disorders. This review is mainly focused on the importance of H2S and NO for normal functioning of CNS. Keywords: Hydrogen sulfide, Nitric oxide, Central nervous system, Gasotransmitters, Gaseous signaling molecules, Neurodegeneration, Neurodegenerative disorders Background Nobel Prizes for Medicine/Physiology in 1998 [7]. Because The discovery of gaseous signaling molecules like H2S, NO, of its toxic nature and noxious effects, beneficial roles of and Carbon monoxide (CO) added a new era in biomedical this molecule were previously neglected [8]. CO was the science as these molecules have great importance in mam- second to be discovered as neurotransmitters, and it has malian physiology [1]. They have been termed as proved its importance in cardiovascular and neuronal func- ‘gasotransmitters’ as they are either internally produced or tioning [9, 10]. However, the recognition of endogenous synthesized (endogenously) in the organism or are received level of H2S in mammalian tissue, confirmed the existence from the atmosphere and transmit chemical signals thereby of this gasotransmitters [11–13]. Synthesis, functions, and promote or induce various physiological changes inside the role of these gasotransmitters in various physiological mammalian body [2]. The term ‘gasotransmitter’ for these aspect is discussed in previous reviews [14–19]. The pri- molecules was firstly introduced in 2002, and these mary purpose of this review is to highlight the contextual molecules share some common characteristics. They are link between CNS and these gaseous signaling molecules. endogenously produced, enzymatically generated, and their production can be regulated. Gasotransmitters are perme- able to the cell membrane, but their functions inside the NO and CNS body are dependent on their concentration [3, 4]. For better NO is synthesized in CNS from an amino acid called as understating and to boost biomedical research in the field L-arginine via an enzyme called NO-synthase (NOS) in of gasotransmitters, a society named European Network on equimolar amounts with L-citrulline [20, 21]. There are Gasotransmitters was established in 2011. three different isoforms of NOS which are genetically Nitricoxidewasthefirstgaseousmoleculetobelinked different [22, 23]. Expression of NOS in various part of with its beneficial roles [5]. NO was the molecule of the the brain is shown in Table 1. Because of its ability to year in 1992 [6]injournal‘Science’ and was recognized by passively permeate cell membrane via diffusion, there is no need of receptor binding unlike conventional neuro- transmitter signaling pathways [24]. Its key potential to * Correspondence: [email protected]; [email protected] 1Otago School of Biomedical Sciences, University of Otago, Dunedin, New Zealand diffuse rapidly in aqueous and lipid environment made it Full list of author information is available at the end of the article unique from other CNS signaling molecules [25]. © The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Panthi et al. Translational Neurodegeneration (2018) 7:3 Page 2 of 8 Table 1 Expression of NOS in various part of brain glutamatergic neurotransmission and acts as a neuromodula- Isoforms of NOS Expression of NOS tor of excitatory neurotransmitter [28, 31]. Recent researches eNOS Vascular endothelium, Choroid plexus also demonstrated the effect of NO on inhibitory GABA- nNOS Neuronal cell bodies especially in thalamus, ergic synaptic transmission [32] via cGMP dependent olfactory bulb, claustrum, amygdala, cortex, suppression of potassium/chloride co-transporter [33]. hippocampus, hypothalamus Reduction of NO may lead to the inability of patients to iNOS Glial cells, Macrophages, Neutrophils learn and memorize due to the impairment of long-term potentiation (LTP), as NO is responsible for the increment NO is mainly produced by Neuronal NO-synthase (nNOS) of the synaptic efficiency of pre-synaptic glutamatergic and Endothelial NO-synthase (eNOS) under normal physio- neurons and this increment induces LTP [34]. This gas- logical conditions, but Inducible NO-synthase (iNOS) is only eous signaling molecule also exerts protective role in generated after induction via inflammatory mediators like cy- brain-ischemia reperfusion injury as a result of its strong tokines and endotoxins [26]. nNOS was the first isoform to stimulatory effect on angiogenesis and vasodilation [35]. be purified and cloned from the brain [27]. NO diffuses from Hemodynamic and vasodilation activity of NO donors [S- one neuron to another. It is not stored in any kind of synap- nitrosoglutathione (GSNO), S-nitroso-N-acetyl-penicillamine tic vesicles, and its release is independent to membrane (SNAP), sodium nitroprusside (SNP), methylamine hexam- depolarization [25, 28]. The generation of NO is similar for ethylene methylamine NONOate (MAHMA), propylamine all subtypes of NOS, but the functional regulation and level propylamine NONOate (PAPA), 3-morpholinosydnonimine of production is different. nNOS and eNOS are constitutive (SIN-1), and nitroglycerin (NTG)] has also provided cerebro- forms of NOS, and both rely on the elevation of intracellular vascular neuroprotective role in the various experimental Ca2+ level to initiate NO synthesis. nNOS requires N- model of stroke [36, 37]. NO produced from endothelial cells methyl-D-aspartate (NMDA) receptor activation, and eNOS and adrenergic neurons regulates cerebral blood flow and needs calmodulin-dependent displacement of regulatory pro- smooth muscle tone during conditions like hypoxia, hyper- teins for NO synthesis. However, iNOS activity is less sensi- capnia, hyperoxia, etc. eNOS mediates the basal release of tive to changes in intracellular Ca2+.But,itcanproducea NO to regulate the cerebral blood flow in various mammals. large amount of NO compared to that of NO associated with This role of NO has been confirmed by various recent eNOS and nNOS [29]. researches using NOS inhibitors [38–40]. The signal transduction of NO in the target cell is associ- Age-related decrease in cGMP was also linked with in- ated with soluble Guanylate cyclase (GC)/Cyclic-guanosine creased NOS level in one recent study which may be helpful mono phosphate (cGMP) (Fig. 1) or with S-nitrosylation of for anti-aging therapies [41]. NO is also suspected to be a protein [30]. NO binds with the cGMP producing enzyme crucial molecule to nitrate/S-nitrosylate brain-derived called as GC and expresses its modulating effects as pre-or neurotrophic factor (BDNF) and tropomyosin-related kinase post-synaptic retrograde messenger which facilitates receptor which helps the maintenance of synaptic plasticity Fig. 1 NO-cGMP signaling pathway: Highly membrane permeable NO binds with NO-soluble Guanylyl cyclase (sGC) which causes conformational changes, and it induces the conversion of GTP-cGMP. cGMP interacts with various intracellular proteins like phosphodiesterase (PDE), cGMP-gated channels (CNG) and protein kinase G (PKG) which stimulates various downstream substrates. Other various pathways are triggered, and many physiological effects starts in cellular level. (Figure adapted and modified from [31]) Panthi et al. Translational Neurodegeneration (2018) 7:3 Page 3 of 8 and LTP [42]. A study has found that NO directly activates reduction of CBF after TBI [56, 57]. Various studies have ryanodine receptor (RyR), which cause the intracellular re- also proved that NO depletion has a critical role in cortical lease of Ca2+ to towards CNS, and it is believed to promote spreading depression, early brain injury, microthrombus the prolonged Ca2+ signaling in the brain. Alike, BDNF and formation, changes in blood flow after subarachnoid tropomyosin-related kinase receptor, this process is also trig- hemorrhage and if we can target this pathway, then it is gered by reversible S-nitrosylation that cause
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